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Year 3 PPT Flashcards > Mental health > Flashcards

Mental health Flashcards

1
Q

Explain the differential diagnoses for a patient presenting with episodic palpitations and dizziness.

A

Panic disorder,
Phobic disorder,
Post-traumatic stress disorder, and Generalized anxiety disorder (GAD).

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2
Q

Define the first-line pharmacological treatment for Generalized Anxiety Disorder (GAD).

A
  • SSRIs

sertraline

escitalopram or paroxetine

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3
Q

what pharmacological options for acute stress reaction

A

CBT or EMDR (eye movement desensitisation and reprocessing therapy

or venlafaxine or SSRI if patient does not want psychological treatment

for sleep issues:
- sleep hygiene
- short term hypnotic

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4
Q

what distinguishes ASR from PTSD

A

will be coined PTSD if persists for longer than 4 weeks

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5
Q

Explain the side effects associated with SSRIs.

A

anxiety, arthralgia, changes in appetite, diarrhea followed by constipation, dizziness, QT interval prolongation, and hyponatremia.

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6
Q

What considerations should be taken into account when prescribing SSRIs?

A

risk of serotonin syndrome, the need for gradual withdrawal, and weighing the risks versus benefits of treatment.
initial increase in suicidal ideation

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7
Q

Describe the role of benzodiazepines in managing anxiety disorders.

A

Benzodiazepines can be used short-term in Generalized Anxiety Disorder (GAD) and other anxiety disorders to provide rapid relief from symptoms.

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8
Q

Explain how benzodiazepines interact with the GABAA receptor.

A

Benzodiazepines bind to a modulatory site on the GABAA receptor, distinct from the GABA-binding site, influencing the receptor’s conformational equilibrium and enhancing its affinity for GABA.

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9
Q

What are the useful effects of benzodiazepines?

A

Benzodiazepines provide sedation, sleep induction, anterograde amnesia, anxiolysis, anticonvulsant activity, and reduction of muscle tone.

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10
Q

How should a patient exhibiting aggressive behaviour be managed according to NICE recommendations?

A

initially physically restrain if possible
seclusion
rapid tranquillisation is last resort

IM lorazepam* or IM haloperidol + promethazine

  • preferred
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11
Q

What risks are associated with the use of benzodiazepines for rapid tranquillisation?

A

loss of consciousness, respiratory depression or arrest, cardiovascular collapse, and potential disinhibition or increased agitation.

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12
Q

Describe the potential complications associated with antipsychotic use.

A

Loss of consciousness, cardiovascular/respiratory complications, collapse, seizures, akathisia, dystonia, dyskinesia, and neuroleptic malignant syndrome.

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13
Q

Define drug dependence in the context of substance abuse.

A

Drug dependence refers to a condition where an individual develops a compulsive need to use a substance, leading to withdrawal symptoms when not using it.

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14
Q

what monitoring is required after RT

A

temp
pulse
BP
hydration
level of consciousness
RR

every 15 mins for at least an hour

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15
Q

features of delirium tremens

A

visual hallucinations, profound confusion, tachycardia, hypertension, hyperthermia, agitation, xs sweating

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16
Q

what drug is used in alcohol withdrawal

A

chlordiazepoxide (is a benzo)
initial dose depends on usual drinking levels/units
dose is gradually reduced

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17
Q

what vitamin supplementation is given in alcohol withdrawal

A
  • high risk = IV pabrinex (B1)

low risk - oral thiamine 100mg

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18
Q

triad of symptoms in WE

A
  • confusion + ataxia
  • ophthalmoplegia
  • memory disturbance
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19
Q

Define the role of opioid agonists in the management of opioid misuse.

A

Opioid agonists suppress craving and withdrawal symptoms, block the acute effects of other opioids, and allow patients to return to a productive lifestyle and address social issues.

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20
Q

examples of opioid agonists

A
  • methadone
  • buprenorphine
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21
Q

How does Methadone differ from Buprenorphine in opioid agonist therapy?

A

Methadone is a long-acting opioid agonist that binds to mu-opioid receptors, while Buprenorphine is a partial mu-opioid agonist, offering less euphoria and sedation.

22
Q

what is naltrexone

A

opioid antagonist

adjunct to prevent relapse in detoxified formerly dependent people

23
Q

What is the purpose of nicotine-replacement therapy in smoking cessation?

A

Nicotine-replacement therapy aims to reduce withdrawal symptoms and is available in various forms such as gum, patches, and sprays.

24
Q

How does Bupropion assist in smoking cessation?

A

Bupropion is a selective dopamine and noradrenaline reuptake inhibitor that likely enhances dopaminergic activity, helping individuals quit smoking.

25
Describe the role of Fomepizol in treating methanol poisoning.
Fomepizol is an antidote used to inhibit the enzyme alcohol dehydrogenase, thereby preventing the conversion of methanol to its toxic metabolites.
26
Define the treatment approach for tricyclic antidepressant overdose.
The treatment for tricyclic antidepressant overdose typically involves administering sodium bicarbonate to counteract metabolic acidosis and stabilize cardiac function.
27
antidote for benzo overdose
flumenazil
28
antidote for methanol overdose
fomepizol
29
antidote for cholinergic overdose
atropine
30
antidote for TCA overdose
sodium bicarb
31
what drugs can be used for managing depression
SSRIs: citalopram, fluoxetine SNRIs: duloxetine, venlafaxine Tricyclics: amitriptyline presynaptic a2 adrenoreceptor blockers = mirtazapine selective noradrenaline reuptake inhibitors = reboxetine MAOIs = phenelzine, selegiline
32
what is the monoamine theory of depression
Low Levels of Monoamines → Depressive Symptoms Serotonin (5-HT): Regulates mood, anxiety, sleep, and appetite. Norepinephrine (NE): Affects energy, alertness, and motivation. Dopamine (DA): Associated with pleasure, reward, and motivation.
33
what is the neurotrophic theory of depression
The neurotrophic hypothesis suggests that depression is linked to reduced levels of brain-derived neurotrophic factor (BDNF) and impaired neuroplasticity in key brain regions, such as the hippocampus and prefrontal cortex. BDNF is a growth factor that supports the survival, growth, and function of neurons. It helps in synaptic plasticity (strengthening of neural connections) and neurogenesis (formation of new neurons). Low BDNF levels are seen in depressed patients, particularly in the hippocampus (important for mood regulation). Stress and the HPA Axis Chronic stress and high cortisol levels (via the hypothalamic-pituitary-adrenal [HPA] axis) can reduce BDNF levels and lead to hippocampal atrophy, worsening depression. This explains why stress is a major trigger for depressive episodes.
34
why are SSRIs often first line
well tolerated reasonably effective safer than TCAs
35
What are the pharmacological choices for managing bipolar disorder?
Lithium Sodium valproate Carbamazepine Lamotrigine Antipsychotics (e.g. Aripiprazole)
36
how does lithium work
inhibits dopamine neurotransmission 💡 Balances excitatory and inhibitory signals in the brain 🔹 Reduces Dopamine (DA) Activity Lithium inhibits dopamine neurotransmission, reducing mania symptoms. Mechanism: Interferes with dopamine receptor sensitivity and release. 🔹 Enhances Serotonin (5-HT) Transmission Increases serotonin levels, improving mood and reducing depression. Mechanism: Increases serotonin release and receptor sensitivity. 🔹 Modulates Glutamate (Excitatory NT) Prevents excessive glutamate activity, which can cause neurotoxicity and mania. Mechanism: Regulates NMDA receptor activity.
37
side effects of Li
nausea, vomiting and diarrhoea tremor thyroid enlargement, sometimes associated with hypothyroidism weight gain hair loss
38
How does Li effect the kidneys
Polyuria (with resulting thirst) resulting from inhibition of the action of antidiuretic hormone and aldosterone. With prolonged treatment, serious renal tubular damage may occur, making it essential to monitor renal function regularly in lithium-treated patients.
39
Symptoms of Li toxicity
Severe tremors, confusion, drowsiness, muscle weakness, vomiting.
40
duration of Li treatment
📌 Lithium is usually a long-term treatment (years). 📌 After first episode, treatment is usually recommended for at least 2 years. 📌 For multiple episodes, it may be lifelong. 📌 Stopping lithium should be gradual (over weeks to months) to prevent relapse.
41
what are the different formulations Li comes in
- standard release tablets - slow release tablets - liquid lithium
42
Li monitoring
Monitoring Schedule (Important!) Blood lithium levels: Every 5–7 days when starting, then every 3 months. Kidney function (eGFR, creatinine): Every 6 months. Thyroid function (TSH, T4): Every 6–12 months. Calcium levels: Every 6–12 months.
43
Li drug interactions
- thiazides - ACEis - ARBS - NSAIDs all above increase lithium levels increasing risk of toxicity as decrease renal clearance by reducing renal perfusion
44
What are the adverse effects of antipsychotic drugs?
weight gain, metabolic syndrome, and cardiovascular issues.
45
What is unique about Clozapine?
only antipsychotic effective in treatment-resistant cases, requiring close monitoring.
46
What are some adverse effects of first generation antipsychotics?
Weight gain/diabetes Prolactin elevation Anticholinergic effects Orthostatic hypotension extrapyramidal SE
47
Which first generation antipsychotic has the highest sedation?
Chlorpromazine
48
examples of typicals
Chlorpromazine fluphenazine haloperidol
49
examples of atypicals
aripiprazole clozapine olanzapine risperidone quetiapine
50
what monitoring is done whilst on anti-psychotics
- FBC, UEs and LFTs baseline + yearly - Lipids and weight: baseline, 3 months+ yearly - fasting glucose: baseline, 4-6 months + yearly - ECG - BP - clozapine (agranulocytosis) weekly for first 18 weeks 18 wks to 1 year = every 2 weeks >1 yr = every 4 weeks

Year 3 PPT Flashcards (4 decks)

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